Wang Heng, Guo Xuan, Wang Xianping, Wang Xiaobo, Chen Jiong
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Nanjing University, 12 Xue-fu Road, Nanjing 210061, China.
State Key Laboratory of Pharmaceutical Biotechnology and MOE Key Laboratory of Model Animals for Disease Study, Model Animal Research Center, Nanjing University, 12 Xue-fu Road, Nanjing 210061, China.
iScience. 2020 Jun 26;23(6):101204. doi: 10.1016/j.isci.2020.101204. Epub 2020 May 27.
During collective cell migration, front cells tend to extend a predominant leading protrusion, which is rarely present in cells at the side or rear positions. Using Drosophila border cells (BCs) as a model system of collective migration, we revealed the presence of a supracellular actomyosin network at the peripheral surface of BC clusters. We demonstrated that the Myosin II-mediated mechanical tension as exerted by this peripheral supracellular network not only mediated cell-cell communication between leading BC and non-leading BCs but also restrained formation of prominent protrusions at non-leading BCs. Further analysis revealed that a cytoplasmic dendritic actin network that depends on the function of Arp2/3 complex interacted with the actomyosin network. Together, our data suggest that the outward pushing or protrusive force as generated from Arp2/3-dependent actin polymerization and the inward restraining force as produced from the supracellular actomyosin network together determine the collective and polarized morphology of migratory BCs.
在集体细胞迁移过程中,前端细胞倾向于伸出一个占主导地位的前沿突起,而侧面或后方位置的细胞很少有这种突起。我们以果蝇边界细胞(BCs)作为集体迁移的模型系统,揭示了在BCs簇的外周表面存在一个超细胞肌动球蛋白网络。我们证明,由这个外周超细胞网络施加的肌球蛋白II介导的机械张力不仅介导了前沿BC和非前沿BC之间的细胞间通讯,还抑制了非前沿BC上突出突起的形成。进一步分析表明,一个依赖于Arp2/3复合体功能的细胞质树突状肌动蛋白网络与肌动球蛋白网络相互作用。总之,我们的数据表明,由Arp2/3依赖性肌动蛋白聚合产生的向外推力或突出力,以及由超细胞肌动球蛋白网络产生的向内约束力,共同决定了迁移BCs的集体和极化形态。